Abstract
Calcium is an essential component in a multitude of cellular processes, ranging from muscle contraction to cell division, and hormone and neurotransmitter release. Disruption of calcium homeostasis at the neuronal level, which occurs in pathological events such as ischaemia, causes a series of biological reactions that ultimately lead to cell death. Furthermore, calcium-triggered events may influence vascular activity, causing spasm at the level of the major vessels and inducing changes in the permeability of the blood-brain barrier. Thus, knowledge of the biochemical events involved in the initiation and progression of cell injury occurring in acute cerebrovascular events may have important implications for possible strategies of pharmacological intervention such as calcium entry blockade.
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